Kinyanjui
Moderator: Prof. Mulimba J. A. O.
22
nd
July 2013
Outline
Definition
Pathophysiology
Aetiology
Presentation
Imaging
Staging
Management
Definition
Cellular death of bone components secondary to
interruption of blood supply
Consequent collapse of bone components
Pain, loss of function of joints
Proximal epiphysis of femur most commonly affected
Pathophysiology
Interruption of blood flow to bone
Affect bones with single terminal blood supply:
Talus
Carpals, tarsals
Proximal humerus
Proximal femur
Femoral condyles
Bone marrow, medullary bone and cortical bone
necrosis results
Final pathway from multiple causes
Predisposing factors
Distance from vascular territory of bone
Enclosed by cartilage limiting vascularity
Endarterioles supply trabelcular bones
Pathways to necrosis
Vascular occlusion direct trauma, stress fracture,
SCD, venous stasis
Intravascular coagulation hypercoaguable states
Primary cell death alcohol, steroids, transplant
patients
Bone necrosis after 12 48 hrs of anoxia
Reactive new bone formation around necrotic bone
Granulation tissue over necrosed bone sclerosis
Structural failure subchondral fracture 1st
Segmental collapse dependant on stress and area of
necrosis
Aetiology
Trauma
Steroids
Alcohol abuse
CT diseases eg SLE
Hematologic (sickle cell disease,
hemoglobinopathies,
thrombophilia)
Metabolic
(hyperlipidemia, gout, renal
failure)
Orthopedic disorders (slipped
capital femoral epiphysis,
developmental dysplasia of the
hip, Legg-Calve-Perthes disease)
Infection (osteomyelitis, HIV])
Renal transplantation
Radiation therapy
Gaucher disease
Malignancy (marrow
infiltration, malignant fibrous
histiocytoma)
Caisson disease
Pregnancy
Bisphosphonate use
Trauma
Severance of blood supply displaced femoral neck
fractures
Scaphoid and talus proximal osteonecrosis due to
distal origin of vessels
Osteoarticular impact localised osteonecrosis in
convex surfaces (osteochondroses)
Non traumatic osteonecrosis
Presentation - History
Trauma
Corticosteroid use
Alcohol intake
Medical conditions malignancy, thrombophilia, SLE, SCD
Pain progressive, severity correlates with size of infarct
Deformity and stiffness later stages
Presentation - examination
Limp
Antalgic gait
Restricted ROM
Tenderness around bone
Joint deformity
Muscle wasting
Imaging: X ray
Initially normal upto 3 months
Sclerosis
Flattening
Subchondral radiolucent lines (cresent sign)
Collapse of cortex
OA
Imaging: CT scan
Used to assess extent of disease and calcification
Clearly shows articular deformity
Calcification and bone collapse
Central sclerosis in femoral head produces asterix sign
Imaging: MRI
90% sensitive
Reduced subchondral intensity on T1 representing
boundary between necrotic and reactive bone
Low signal on T1 and high signal on T2 reactive zone
(diagnostic)
Changes detected early
Radionuclide scan
Donut sign central reduced uptake with surrounding
rim of increased uptake
More sensitive than plain films in early AVN
Less sensitive than MRI
Necrotic zone surrounded by reactive new bone
formation
Histology
Definitive diagnosis
Usually retrospective/confirmatory during surgery for
treatment
Occasionally biopsy of sclerotic lesion
Necrosis of cortical bone is followed by a regenerative
process in surrounding tissues.
Increased osteoclastic activity to remove necrotic bone
and increased osteoblastic activity as a reparative
process
Intramedullary pressures
Cannula into metaphysis
Measure at rest and after saline injection
Femoral head:
10 20 mmHg, increasing by 15 mmHg after saline
Markedly increased values in AVN (3 to 4 fold)
Less marked increase in OA
ARCO Staging
Stage Clinical and radiological findings
0 Asymptomatic, radiology normal, histological diagnosis
I +-symptoms, normal CT and X ray, early changes on MRI
II Symptomatic, bone density changes on X ray, diagnostic MRI findings
III Cresent sign. IIIa - <15% articular surface, IIIb 15 30%, IIIc >30%
IV Collapse of head IVa - <15% surface collapsed, IVb 15 30%. IVc >30%
V OA narrowed joint space, acetabular sclerosis, marginal osteophytes
VI Extensive destruction of joint and involved bone
Management principles
Early stages (I & II):
Bisphosphonates prevent collapse
Unloading osteotomies
Medullary decompression + bone grafting
Intermediate stage (III & IV):
Realignment osteototmies, decompression
Arthrodesis
Late stage (V & VI):
Analgesia, activity modification
Arthrodesis
Arthroplasties
Management - conservative
Offloading affected joints with use of crutches
Immobilisation
Analgesia
Bisphosphonates to delay femoral head collapse
Statins in patients on high dose corticosteroids
reduced lipid deposition
Core decompression
Indicated in ARCO I and II
8 10 mm anterolateral core of bone
Filled with bone graft (vascularised/non vascularised)
Decompresses medullary cavity, reduces pain
Cortical (osteoconductive) or cancellous(osteoinductive)
bone graft
Vascularised graft may reverse necrosis
Realignment osteotomy
Indicated in ARCO III & IV
Used to relocate necrotic area from weight bearing portion
of femoral head
Angular osteotomies more common
Multiple techniques for holding the fixation
Sugano intertrochanteric rotational osteotomy technically
demanding but higher success rate
Arthroplasty
Indicated in ARCO IV onwards
Main aim is pain reduction
Young patients will need revision
Higher failure rates than in OA
Hemi arthroplasty an option
Eponymous syndromes
Kienbocks disease idiopathic avascular necrosis of
the lunate bone that leads to collapse and progressive
carpal arthritis. PRC as treatment
Legg-Calve-Perthess idiopathic osteonecrosis of
femoral capital epiphysis in children. Treated with
orthotics, traction, surgery to rotate the femoral head
Preiser's disease idiopathic osteonecrosis of
scaphoid. Collapse with progressive arthritis. PRC,
Excision and fusion,
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